The type I interferon (IFN), IFN beta (IFN beta), is the only FDA- approved immunotherapeutic for the treatment of multiple sclerosis (MS), but unfortunately causes toxic side effects. Another type I IFN, IFNtau, originally identified for its pregnancy recognition role in ruminants, has been found to have similar positive activities to the other type I IFNs. In addition, ovine IFNtau has been shown to block the development of experimental allergic encephalomyelitis (EAE), an animal model for MS, but without the associated toxicity of bone marrow suppression and weight loss. Since expression of a human IFNtau has not been successful, a chimeric IFN has been constructed that consists of amino acid residues 1- 27 from ovine IFNtau and residues 28-166 from human IFNalphaD. Using the PL/J and SJL/J mouse EAE models, this chimeric IFN will be tested for its ability to protect mice against the induction of EAE, superantigen reactivation of EAE, and protection against relapsing and remitting symptoms of EAE. The chimeric IFN may provide a non-toxic alternative to IFNbeta therapy for MS without inducing a strong immune response in humans. Further, successful treatment with the ovine IFNtau/human IFNalphaD chimeric IFN would aid in improved therapy of other IFN treated diseases. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE